Institute for Transformative Molecular Medicine, Department of Medicine, Case Western Reserve University and University Hospitals, Cleveland, Ohio, USA.
Transfusion. 2011 Apr;51(4):852-8. doi: 10.1111/j.1537-2995.2011.03097.x.
Protein S-nitrosylation (the binding of a nitric oxide [NO] group to a cysteine thiol) is a major mechanism through which the ubiquitous cellular influence of NO is exerted. Disruption of S-nitrosylation is associated with a wide range of pathophysiologic conditions. Hemoglobin (Hb) exemplifies both of these concepts. It is the prototypical S-nitrosylated protein in that it binds, activates, and deploys NO. Within red blood cells (RBCs), Hb is S-nitrosylated during the respiratory cycle and thereby conveys NO bioactivity that may be dispensed to regulate local blood flow in the physiologic response known as hypoxic vasodilation. Hb thus both delivers oxygen directly and delivers vasoactivity to potentially optimize tissue perfusion in concert with local metabolic demand. Accordingly, decreased levels of S-nitrosylated Hb (also known as S-nitrosohemoglobin) and/or impaired delivery of RBC-derived NO bioactivity have been observed in a variety of disease states that are characterized by tissue hypoxemia. It has been shown recently that storage of blood depletes S-nitrosylated Hb, accompanied by reduced ability of RBCs to induce vasodilation. This defect appears to account in significant part for the impaired ability of banked RBCs to deliver oxygen. Renitrosylation can correct this impairment and thus may offer a means to ameliorate the disruptions in tissue perfusion produced by transfusion.
蛋白质 S-亚硝基化（一氧化氮 [NO] 基团与半胱氨酸巯基的结合）是 NO 对细胞普遍影响的主要机制之一。S-亚硝基化的破坏与广泛的病理生理状况有关。血红蛋白 (Hb) 就是这两个概念的典型代表。它是典型的 S-亚硝基化蛋白，能结合、激活和部署 NO。在红细胞 (RBC) 中，Hb 在呼吸循环过程中发生 S-亚硝基化，从而传递可能用于调节缺氧性血管舒张等生理反应中局部血流的 NO 生物活性。因此，Hb 既能直接输送氧气，又能输送血管活性物质，以与局部代谢需求相协调，从而优化组织灌注。因此，在各种以组织缺氧为特征的疾病状态中，观察到 S-亚硝基化 Hb（也称为 S-亚硝基血红蛋白）水平降低和/或 RBC 衍生的 NO 生物活性的输送受损。最近有研究表明，血液储存会消耗 S-亚硝基化 Hb，同时 RBC 诱导血管舒张的能力也会降低。这一缺陷似乎在很大程度上解释了储存 RBC 输送氧气能力受损的原因。再亚硝基化可以纠正这种损伤，从而可能提供一种改善输血引起的组织灌注障碍的方法。
